Kidney disease that reduces glomerular filtration and fails to excrete the acids produced in metabolism (uremic acidosis). Prolonged vomiting that loses the alkaline contents of the upper intestine and stomach contents. (Losing only the stomach contents produces metabolic alkalosis.) Prolonged diarrhea, in which excess alkaline intestinal secretions are lost (especially in infants).

Diabetes mellitus, in which some fatty acids are converted into ketone bodies. These ketone bodies include acetoacetic acid, beta-hydroxybutyric acid, and acetone. Normally these molecules are produced in relatively small quantities, and cells oxidize them as energy sources. However, if fats are being utilized at an abnormally high rate, as may occur in diabetes mellitus, ketone bodies may accumulate faster than they can be oxidized. At such

Failure of kidneys to excrete acids

Decreased gas exchange times, these compounds may be excreted in the urine (ketonuria); in addition, acetone, which is volatile, may be excreted by the lungs and impart a fruity odor to the breath. More seriously, the accumulation of acetoacetic acid and beta-hydroxybutyric acid may lower pH (ketonemic acidosis).

These acids may also combine with bicarbonate ions in the urine. As a result, excess bicarbonate ions are excreted, interfering with the function of the bicarbonate acid-base buffer system.

In each case, the pH tends to shift toward lower values. However, the following factors resist this shift: chemical buffer systems, which accept excess hydrogen ions; the respiratory center, which increases the breathing rate and depth; and the (continued)

Excessive production of acidic ketones as in diabetes mellitus

Accumulation of nonrespiratory auids

Metabolic acidosis

Figure 21F

Some of the factors that lead to metabolic acidosis.

Figure 21E

Some of the factors that lead to respiratory acidosis.

Figure 21F

Some of the factors that lead to metabolic acidosis.

Acid-Base Imbalances (continued]

kidneys, which excrete more hydrogen ions.

Respiratory alkalosis develops as a result of hyperventilation, described in chapter 19 (p. 803). Hyperventilation is accompanied by too great a loss of carbon dioxide and consequent decreases in carbonic acid and hydrogen ion concentrations (fig. 21G).

Hyperventilation may occur during periods of anxiety, although it may also accompany fever or poisoning from salicylates, such as aspirin. At high altitudes, hyperventilation may be a response to low oxygen pressure.




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